Two independent experiments were performed with three groups each (sepsis control, sepsis, and sepsis with apoE23 treatment) to investigate the anti-inflammatory effect of apolipoprotein 23 (apoE23) in a mouse model of sepsis induced by . Survival rates; plasma level variations in tumor necrosis factor (TNF)-α, interleukin (IL)-6, and lipopolysaccharide (LPS); S. colony-forming units in the spleen tissue; and mRNA and protein expression levels of low-density lipoprotein receptor (LDLR), LDLR-related protein (LRP), syndecan-1, and scavenger receptor B1 were evaluated in the livers of mice from the three groups. Results found that the survival rate of septic mice treated with apoE23 was 100% within 48 h, while it was only 40% in septic mice without apoE23 treatment ( < 0.001). The plasma LPS, TNF-α, and IL-6 levels and the load in mice in the apoE23-treated group were significantly lower than those in septic mice ( < 0.05). Moreover, apoE23 restored the downregulated expression of LDLR and LRP in the liver tissue of septic mice. So apoE23 exhibits an anti-inflammatory effect in the mouse model of -induced sepsis. Further studies are required to understand the mechanisms underlying the anti-inflammatory effects of apoE23.
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http://dx.doi.org/10.1515/med-2023-0767 | DOI Listing |
Immunopharmacol Immunotoxicol
February 2025
Nutrition Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Septic shock involves severe systemic inflammatory reaction toward various invading species, such as microorganisms and microbial toxins. Such a response is complicated and characterized as being a dynamic and time-dependent phenomenon. During this response, a significant amount of pro-inflammatory cytokines may be produced, causing a rapid death rate in septic victims and occasionally leading to apoptosis of immune cells within the first hours of septic reaction.
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Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Introduction: Septic arthritis, primarily caused by (), is a severe joint infection that leads to joint and bone damage. lipoproteins (LPPs) bind to Toll-like Receptor 2 (TLR2), inducing arthritis and localized bone loss. Aging affects TLR2 immune response to pathogens.
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January 2025
Department of Psychiatry, University of Florida, Gainesville, FL 32610, USA; McKnight Brain Institute, University of Florida, Gainesville, FL 32610, USA. Electronic address:
Int Immunopharmacol
December 2024
Department of Trauma-Emergency & Critical Care Medicine, Shanghai Fifth People's Hospital, Fudan University, 128 Ruili Road, Shanghai 200240, China. Electronic address:
Sepsis is the leading cause of death among critically ill patients in clinical practice, making it urgent to reduce its incidence and mortality rates. In sepsis, macrophage dysfunction often worsens and complicates the condition. M1 and M2 macrophages, two distinct types, contribute to pro-inflammatory and anti-inflammatory effects, respectively.
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December 2024
National clinical research center for hematologic diseases, Jiangsu Institute of Hematology, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, 215006, China; Institute of Blood and Marrow Transplantation, Collaborative Innovation Center of Hematology, Soochow University, Suzhou, Jiangsu, 215006, China; Key Laboratory of Thrombosis and Hemostasis of Ministry of Health, Suzhou, 215006, China; State Key Laboratory of Radiation Medicine and Protection, Soochow University, Suzhou, Jiangsu, 215006, China. Electronic address:
Sepsis-induced thrombocytopenia (SIT) is a widely accepted predictor of poor prognosis during sepsis, while the mechanism of SIT remains elusive. In this study, we revealed that SIT patients and septic mice exhibited higher levels of pro-inflammatory macrophages and phosphorylated BTK (p-BTK) expression in macrophages, which were closely correlated with platelet counts. Treatment with the BTK inhibitor, BGB-3111 in SIT mice resulted in enhanced production of megakaryocytes and platelets.
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